Aging-US

A new research paper was published on the cover of Aging (Aging-US) Volume 15, Issue 4, entitled, “Relationship between telomere shortening and early subjective depressive symptoms and cognitive complaints in older adults.” Telomere length (TL) has been reported to be associated with depression and cognitive impairment in elderly. Early detection of depression and cognitive impairment is important to delay disease progression. Therefore, in this new study, researchers Myung-Hoon Han, Eun-Hye Lee2, Hyun-Hee Park, Seong Hye Choi, and Seong-Ho Koh from Hanyang University and Inha University aimed to identify whether TL is associated with early subjective depressive symptoms and cognitive complaints among healthy elderly subjects. “Several hypotheses have been proposed to explain the emergence of a prematurely aged phenotype in late-life depression, such as glucocorticoid cascade dysregulation, increased allostatic load, and telomere shortening [10, 12].” This study was a multicenter, outcome assessor-blinded, 24-week, randomized controlled trial (RCT). Measurement of questionnaire and physical activity scores and blood sample analyses were performed at baseline and after six months of follow-up in all study participants. Linear regression analyses were performed to identify whether early subjective depressive symptoms, cognitive complaints, and several blood biomarkers are associated with TL. Altogether, 137 relatively healthy elderly individuals (60–79 years old) were enrolled in this prospective RCT. The team observed an approximate decrease of 0.06 and 0.11−0.14 kbps of TL per one point increase in the geriatric depression scale and cognitive complaint interview scores, respectively, at baseline and after six months of follow-up. They also found an approximate decrease of 0.08−0.09 kbps of TL per one point increase in interleukin (IL)-6 levels at baseline and after six months of follow-up. “In conclusion, we showed that both early subjective depressive symptoms and cognitive complaints in relatively healthy elderly individuals were associated with a relatively shorter TL in the randomized controlled prospective SUPERBRAIN study. In addition, a shorter TL was associated with increased IL-6 levels in our study participants. We believe that IL-6, an inflammatory cytokine, plays an important role in the relationship of shortening TL with early subjective depressive mood and cognitive complaints. Although the results will need to be verified through a large-scale RCT in the future, we believe that our findings will help prevent and treat depression and cognitive impairment in the healthy elderly.” DOI: https://doi.org/10.18632/aging.204533 Corresponding Authors: Seong Hye Choi - seonghye@inha.ac.kr, Seong-Ho Koh - ksh213@hanyang.ac.kr Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204533 Keywords - aging, telomere length, cognitive complaint, depressive symptom, interleukin-6 About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ MEDIA@IMPACTJOURNALS.COM

Listen to a blog summary of a trending research paper published in Volume 15, Issue 3 of Aging (Aging-US), entitled, "The lipidomes of C. elegans with mutations in asm-3/acid sphingomyelinase and hyl-2/ceramide synthase show distinct lipid profiles during aging." __________________________________________________ Lipids are a diverse group of biomolecules that are essential for life, including fats, oils, waxes, and steroids, and play crucial roles in cell membrane structure, energy storage and signaling. Lipidomics is the comprehensive analysis of lipids and their interactions in biological systems, with an aim to understand the role of lipids in cellular processes and their association with diseases. As we age, our cells undergo complex changes, including alterations in cellular lipid profiles. These changes are not only confined to humans; organisms such as the nematode Caenorhabditis elegans (C. elegans) are also subject to changes in lipid composition during aging. “For example, lipid classes including fatty acids (FA), triacylglycerols (TAG), sphingolipids (SL), and phospholipids (PL) have been identified as targets in lipid signatures related to aging [2, 3]. Furthermore, specific signatures are detected in the lipid profiles of those with age-related diseases, such as Alzheimer’s Disease [4–9]. In addition, the abundance of many fatty acid subtypes differs between the youth, elderly, and centenarians [10, 11].” In a recent study, researchers Trisha A. Staab, Grace McIntyre, Lu Wang, Joycelyn Radeny, Lisa Bettcher, Melissa Guillen, Margaret P. Peck, Azia P. Kalil, Samantha P. Bromley, Daniel Raftery, and Jason P. Chan from Marian University, the University of Washington and Juniata College investigate the lipid profiles of C. elegans with mutations in the genes asm-3/acid sphingomyelinase and hyl-2/ceramide synthase during aging. On February 13, 2023, their research paper was published in Aging’s Volume 15, Issue 3, entitled, “The lipidomes of C. elegans with mutations in asm-3/acid sphingomyelinase and hyl-2/ceramide synthase show distinct lipid profiles during aging.” Full blog - https://aging-us.org/2023/02/the-role-of-lipids-in-aging-insights-from-c-elegans/ DOI - https://doi.org/10.18632/aging.204515 Corresponding author - Jason P. Chan - jpchan@me.com Keywords - lipidomics, aging, sphingolipid metabolism, C. elegans, fatty acid metabolism About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

A new research paper was published in Aging (listed as "Aging (Albany NY)" by MEDLINE/PubMed and "Aging-US" by Web of Science) Volume 15, Issue 3, entitled, “Metformin use history and genome-wide DNA methylation profile: potential molecular mechanism for aging and longevity.” Metformin, a commonly prescribed anti-diabetic medication, has repeatedly been shown to hinder aging in pre-clinical models and to be associated with lower mortality for humans. It is, however, not well understood how metformin can potentially prolong lifespan from a biological standpoint. In this recent study, researchers Pedro S. Marra, Takehiko Yamanashi, Kaitlyn J. Crutchley, Nadia E. Wahba, Zoe-Ella M. Anderson, Manisha Modukuri, Gloria Chang, Tammy Tran, Masaaki Iwata, Hyunkeun Ryan Cho, and Gen Shinozaki from Stanford University School of Medicine, University of Iowa, Tottori University Faculty of Medicine, University of Nebraska Medical Center College of Medicine, and Oregon Health and Science University School of Medicine hypothesized that metformin’s potential mechanism of action for longevity is through its epigenetic modifications. “To test our hypothesis, we conducted a post-hoc analysis of available genome-wide DNA methylation (DNAm) data obtained from whole blood collected from inpatients with and without a history of metformin use.” The researchers assessed the methylation profile of 171 patients (first run) and only among 63 diabetic patients (second run) and compared the DNAm rates between metformin users and nonusers. Enrichment analysis from the Kyoto Encyclopedia of Genes and Genome (KEGG) showed pathways relevant to metformin’s mechanism of action, such as longevity, AMPK and inflammatory pathways. They also identified several pathways related to delirium whose risk factor is aging. Moreover, top hits from the Gene Ontology (GO) included HIF-1α pathways. However, no individual CpG site showed genome-wide statistical significance (p < 5E-08). “This study may elucidate metformin’s potential role in longevity through epigenetic modifications and other possible mechanisms of action.” Read the Full Paper: DOI: https://doi.org/10.18632/aging.204498 Corresponding Author: Gen Shinozaki - gens@stanford.edu Keywords: metformin, longevity, diabetes, epigenetics, aging, inflammation, methylation Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204498 About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Crossref is a non-profit organization that logs and updates citations for scientific publications. Below are Crossref’s Top 10 Aging DOIs in 2022. 10: DNA- and telomere-damage does not limit lifespan: evidence from rapamycin DOI: https://doi.org/10.18632/aging.202674 Author: Mikhail V. Blagosklonny 9: Psychological factors substantially contribute to biological aging: evidence from the aging rate in Chinese older adults DOI: https://doi.org/10.18632/aging.204264 Authors: Fedor Galkin, Kirill Kochetov, Diana Koldasbayeva, Manuel Faria, Helene H. Fung, Amber X. Chen, and Alex Zhavoronkov 8: DNA methylation GrimAge strongly predicts lifespan and healthspan DOI: https://doi.org/10.18632/aging.101684 Authors: Ake T. Lu, Austin Quach, James G. Wilson, Alex P. Reiner, Abraham Aviv, Kenneth Raj, Lifang Hou, Andrea A. Baccarelli, Yun Li, James D. Stewart, Eric A. Whitsel, Themistocles L. Assimes, Luigi Ferrucci, and Steve Horvath 7: Hallmarks of aging-based dual-purpose disease and age-associated targets predicted using PandaOmics AI-powered discovery engine DOI: https://doi.org/10.18632/aging.203960 Authors: Frank W. Pun, Geoffrey Ho Duen Leung, Hoi Wing Leung, Bonnie Hei Man Liu, Xi Long, Ivan V. Ozerov, Ju Wang, Feng Ren, Alexander Aliper, Evgeny Izumchenko, Alexey Moskalev, João Pedro de Magalhães, and Alex Zhavoronkov 6: CircRNA_100367 regulated the radiation sensitivity of esophageal squamous cell carcinomas through miR-217/Wnt3 pathway DOI: https://doi.org/10.18632/aging.102580 Authors: Junqi Liu, Nannan Xue, Yuexin Guo, Kerun Niu, Liang Gao, Song Zhang, Hao Gu, Xin Wang, Di Zhao, and Ruitai Fan 5: Five years of exercise intervention at different intensities and development of white matter hyperintensities in community dwelling older adults, a Generation 100 sub-study DOI: https://doi.org/10.18632/aging.203843 Authors: Anette Arild, Torgil Vangberg, Hanne Nikkels, Stian Lydersen, Ulrik Wisløff, Dorthe Stensvold, and Asta K. Håberg 4: The aging-related risk signature in colorectal cancer DOI: https://doi.org/10.18632/aging.202589 Authors: Taohua Yue, Shanwen Chen, Jing Zhu, Shihao Guo, Zhihao Huang, Pengyuan Wang, Shuai Zuo, and Yucun Liu 3: An epigenetic biomarker of aging for lifespan and healthspan DOI: https://doi.org/10.18632/aging.101414 Authors: Morgan E. Levine, Ake T. Lu, Austin Quach, Brian H. Chen, Themistocles L. Assimes, Stefania Bandinelli, Lifang Hou, Andrea A. Baccarelli, James D. Stewart, Yun Li, Eric A. Whitsel, James G Wilson, Alex P Reiner, Abraham Aviv, Kurt Lohman, Yongmei Liu, Luigi Ferrucci, and Steve Horvath 2: Nrf2 inhibits ferroptosis and protects against acute lung injury due to intestinal ischemia reperfusion via regulating SLC7A11 and HO-1 DOI: https://doi.org/10.18632/aging.103378 Authors: Hui Dong, Zhuanzhuan Qiang, Dongdong Chai, Jiali Peng, Yangyang Xia, Rong Hu, and Hong Jiang 1: Optimizing future well-being with artificial intelligence: self-organizing maps (SOMs) for the identification of islands of emotional stability DOI: https://doi.org/10.18632/aging.204061 Authors: Fedor Galkin, Kirill Kochetov, Michelle Keller, Alex Zhavoronkov, and Nancy Etcoff ____________________ About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​.

A new research paper was published in Aging (listed as "Aging (Albany NY)" by MEDLINE/PubMed and "Aging-US" by Web of Science) Volume 15, Issue 3, entitled, “Epigenetic age and lung cancer risk in the CLUE II prospective cohort study.” Epigenetic age, a robust marker of biological aging, has been associated with obesity, low-grade inflammation and metabolic diseases. However, few studies have examined associations between different epigenetic age measures and risk of lung cancer, despite great interest in finding biomarkers to assist in risk stratification for lung cancer screening. In a recent study, researchers Dominique S. Michaud, Mei Chung, Naisi Zhao, Devin C. Koestler, Jiayun Lu, Elizabeth A. Platz, and Karl T. Kelsey from Tufts University, University of Kansas Medical Center, Johns Hopkins Bloomberg School of Public Health, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, and Brown University conducted a nested case-control analysis of 208 lung cancer cases and 208 matched controls with archived pre-diagnostic blood samples (from 1989). The case-control study is nested in the CLUE II cohort study, a predominantly White cohort of men and women, based in Maryland, USA. “It is important to examine whether epigenetic age is associated with lung cancer risk across multiple prospective studies to determine its utility as a potential biomarker to be considered for risk stratification in the selection of high-risk individuals for lung cancer screening.” Prediagnostic blood samples were collected in 1989 (CLUE II study baseline) and stored at −70°C. DNA was extracted from buffy coat and DNA methylation levels were measured using Illumina MethylationEPIC BeadChip Arrays. Three epigenetic age acceleration (i.e., biological age is greater than chronological age) measurements (Horvath, Hannum and PhenoAge) were examined in relation to lung cancer risk using conditional logistic regression. The researchers did not observe associations between the three epigenetic age acceleration measurements and risk of lung cancer overall; however, inverse associations for the two Hannum age acceleration measures (intrinsic and extrinsic) were observed in men and among younger participants, but not in women or older participants. Additionally, they did not observe effect modification by time from blood draw to diagnosis. “Findings from this study do not support a positive association between three different biological age acceleration measures and risk of lung cancer. Additional studies are needed to address whether epigenetic age is associated with lung cancer in never smokers.” Read the Full Paper: DOI: https://doi.org/10.18632/aging.204501 Corresponding Author: Dominique S. Michaud - Dominique.Michaud@tufts.edu Keywords: DNA methylation, epigenetic clocks, lung cancer, cohort study Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204501 About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/

A new research paper was published on the cover of Aging (listed as "Aging (Albany NY)" by Medline/PubMed and "Aging-US" by Web of Science) Volume 15, Issue 3, entitled, “Immune-mediated platelet depletion augments Alzheimer’s disease neuropathological hallmarks in APP-PS1 mice.” In Alzheimer’s disease (AD), platelets become dysfunctional and might contribute to amyloid beta deposition. In a recent study, researchers Diana M. Bessa de Sousa, Ariane Benedetti, Barbara Altendorfer, Heike Mrowetz, Michael S. Unger, Katharina Schallmoser, Ludwig Aigner, and Kathrin Maria Kniewallner from Paracelsus Medical University and Austrian Cluster for Tissue Regeneration in Austria depleted platelets in one-year-old APP Swedish PS1 dE9 (APP-PS1) transgenic mice for five days, using intraperitoneal injections of an anti-CD42b antibody, and assessed changes in cerebral amyloidosis, plaque-associated neuritic dystrophy and gliosis. “The potential role of platelets in amyloid beta deposition led to the hypothesis that reducing platelet numbers might ameliorate AD pathology [30]. Here, we performed immune-mediated platelet depletion in APP-PS1 mice with an already fully developed amyloidosis and investigated its effects on classical hallmarks of AD: amyloid plaque pathology, plaque-associated neuritic dystrophy and gliosis.” In APP-PS1 female mice, platelet depletion shifted amyloid plaque size distribution towards bigger plaques and increased neuritic dystrophy in the hippocampus. In platelet-depleted females, plaque-associated Iba1+ microglia had lower amounts of fibrillar amyloid beta cargo and GFAP+ astrocytic processes showed a higher overlap with thioflavin S+ amyloid plaques. In contrast to the popular hypothesis that platelets foster plaque pathology, data from this study suggest that platelets might limit plaque growth and attenuate plaque-related neuritic dystrophy at advanced stages of amyloid plaque pathology in APP-PS1 female mice. Whether the changes in amyloid plaque pathology are due to a direct effect on amyloid beta deposition or are a consequence of altered glial function needs to be further elucidated. “In APP-PS1 females, acute thrombocytopenia aggravates AD neuropathology, suggesting that platelets might have a protective function in AD. However, the underlying molecular mechanisms by which platelets modulate amyloid plaque deposition remain elusive and need to be investigated in future experiments.” DOI: https://doi.org/10.18632/aging.204502 Corresponding Author: Kathrin Maria Kniewallner - kathrin.drerup@pmu.ac.at Keywords: Alzheimer’s disease, platelets, amyloid-beta, microglia, astrocytes Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204502 About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Blog summary of "Epigenetic age acceleration correlates with BMI in young adults" published in Volume 15, Issue 2 of Aging (Aging-US). ___________________________________________ While the study of genetics focuses on heredity and alterations in the genetic code itself, epigenetics refers to the changes in gene expression that occur as a result of environmental or lifestyle factors. Advances in epigenetic research have allowed measures of DNA methylation (DNAm) (epigenetic clocks) to illustrate clear links between obesity, accelerated epigenetic aging and a variety of negative health outcomes in older adults. Despite these advances, there is a lack of research about these correlations and sex-based variations among young adults. The ability to detect accelerated epigenetic aging in young adulthood could potentially be used to prevent the onset of chronic diseases and improve health outcomes later in life. “Moreover, few studies have included replication across measures of obesity and epigenetic aging to examine the robustness or specificity of these effects. Finally, little is known about sex differences in the links between obesity and epigenetic aging, despite evidence of substantial sex dimorphism in both physiological and epigenetic aging [20].” In a recent study, researchers Christy Anne Foster, Malcolm Barker-Kamps, Marlon Goering, Amit Patki, Hemant K. Tiwari, and Sylvie Mrug from the University of Alabama at Birmingham’s Department of Pediatrics examined the relationship between obesity and measures of DNAm in young adults. They also investigated whether there is a sex-dependant correlation between obesity and DNAm in young adults. On January 18, 2023, their research paper was published in Aging’s Volume 15, Issue 2, and entitled, “Epigenetic age acceleration correlates with BMI in young adults.” Full blog - https://aging-us.org/2023/02/bmi-correlates-with-accelerated-epigenetic-aging-in-young-adults/ DOI - https://doi.org/10.18632/aging.204492 Corresponding author - Christy Anne Foster - cafoster@uabmc.edu Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204492 Keywords - obesity, epigenetic aging, young adult, DNA methylation, epigenetic acceleration About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://youtube.com/Aging-US LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

A new research paper was published in Aging (listed as "Aging (Albany NY)" by MEDLINE/PubMed and "Aging-US" by Web of Science) Volume 15, Issue 2, entitled, “Body weight influences musculoskeletal adaptation to long-term voluntary wheel running during aging in female mice.” Aging increases the prevalence of sarcopenia and osteoporosis that are often both components of a musculoskeletal syndrome, osteosarcopenia. Osteosarcopenia is highly associated with frailty, falls, fractures, and disability, leading to decreased quality of life and increased morbidity and mortality. Frailty is the hallmark of aging that can be delayed with exercise. In this new research paper, researchers Yukiko Kitase, Julian A. Vallejo, Sarah L. Dallas, Yixia Xie, Mark Dallas, LeAnn Tiede-Lewis, David Moore, Anthony Meljanac, Corrine Kumar, Carrie Zhao, Jennifer Rosser, Marco Brotto, Mark L. Johnson, Ziyue Liu, Michael J. Wacker, and Lynda Bonewald from Indiana University, University of Missouri and University of Texas wrote that the present studies were initiated based on the hypothesis that long-term voluntary wheel running (VWR) in female mice from 12 to 18 or 22 months of age would have beneficial effects on the musculoskeletal system. “Frequently osteoporosis and sarcopenia occur concurrently. It is not known if one precedes the other or if one condition influences disease progression of the other condition [26, 27]. We hypothesized that long-term voluntary exercise started later in life (12 months of age) would improve both skeletal muscle and bone parameters in aging female mice up to 22 months.” Mice were separated into high (HBW) and low (LBW) body weight based on final body weights upon termination of experiments. Bone marrow fat was significantly higher in HBW than LBW under sedentary conditions, but not with VWR. HBW was more protective for soleus size and function than LBW under sedentary conditions, however VWR increased soleus size and function regardless of body weight. VWR plus HBW was more protective against muscle loss with aging. Similar effects of VWR plus HBW were observed with the extensor digitorum longus, EDL, however, LBW with VWR was beneficial in improving EDL fatigue resistance in 18 mo mice and was more beneficial with regards to muscle production of bone protective factors. VWR plus HBW maintained bone in aged animals. In summary, HBW had a more beneficial effect on muscle and bone with aging especially in combination with exercise. These effects were independent of bone marrow fat, suggesting that intrinsic musculoskeletal adaptions were responsible for these beneficial effects.” “Collectively, VWR has beneficial effects on bone health during advanced aging regardless of body weight, but VWR differentially alters bone parameters depending on body weight, with modifications in mechanical properties in LBW but structural modifications in HBW contributing to the prevention of osteopenia.” Full Paper: DOI: https://doi.org/10.18632/aging.204390 Corresponding Authors: Lynda Bonewald -bonewal@iu.edu, Michael J. Wacker - wackerm@umkc.edu About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Website - https://www.Aging-US.com SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://youtube.com/Aging-US LinkedIn - https://www.linkedin.com/company/aging/

A new research perspective was published in Aging (listed as "Aging (Albany NY)" by MEDLINE/PubMed and "Aging-US" by Web of Science) Volume 15, Issue 2, entitled, “Are menopause, aging and prostate cancer diseases?” In this new research perspective, researcher Mikhail (Misha) Blagosklonny M.D., Ph.D., from Roswell Park Comprehensive Cancer Center wrote in the abstract: “There is no doubt that prostate cancer is a disease. Then, according to hyperfunction theory, menopause is also a disease. Like all age-related diseases, it is a natural process, but is also purely harmful, aimless and unintended by nature. But exactly because these diseases (menopause, prostate enlargement, obesity, atherosclerosis, hypertension, diabetes, presbyopia and thousands of others) are partially quasi-programmed, they can be delayed by slowing aging. Is aging a disease? Aging is a quasi-programmed disease that is partially treatable by rapamycin. On the other hand, aging is an abstraction, a sum of all quasi-programmed diseases and processes. In analogy, the zoo consists of animals and does not exist without animals, but the zoo is not an animal.” Read the Full Paper: DOI: https://doi.org/10.18632/aging.204499 Corresponding Author: Mikhail V. Blagosklonny Corresponding Emails: Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com Keywords: geroscience, mTOR, hyperfunction theory of aging, lifespan, healthspan Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204499 About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://youtube.com/Aging-US LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

A new research paper was published on the cover of Aging (Aging-US)) Volume 15, Issue 2, entitled, “Clearance of p16Ink4a-positive cells in a mouse transgenic model does not change β-cell mass and has limited effects on their proliferative capacity.” Type 2 diabetes is partly characterized by decreased β-cell mass and function which have been linked to cellular senescence. Despite a low basal proliferative rate of adult β-cells, they can respond to growth stimuli, but this proliferative capacity decreases with age and correlates with increased expression of senescence effector, p16Ink4a. In a new study, researchers Nadine Bahour, Lucia Bleichmar, Cristian Abarca, Emeline Wilmann, Stephanie Sanjines, and Cristina Aguayo-Mazzucato from the Joslin Diabetes Center at Harvard Medical School hypothesized that selective deletion of p16Ink4a-positive cells would enhance the proliferative capacity of the remaining β-cells due to the elimination of the local senescence-associated secretory phenotype (SASP). “We aimed to investigate the effects of p16Ink4a-positive cell removal on the mass and proliferative capacity of remaining β-cells using INK-ATTAC mice as a transgenic model of senolysis.” Clearance of p16Ink4a-positive subpopulation was tested in mice of different ages, males and females, and with two different insulin resistance models: high-fat diet (HFD) and insulin receptor antagonist (S961). Clearance of p16Ink4a-positive cells did not affect the overall β-cell mass. β-cell proliferative capacity negatively correlated with cellular senescence load and clearance of p16Ink4a positive cells in 1-year-old HFD mice improved β-cell function and increased proliferative capacity in a subset of animals. Single-cell sequencing revealed that the targeted p16Ink4a subpopulation of β-cells is non-proliferative and non-SASP producing whereas additional senescent subpopulations remained contributing to continued local SASP secretion. “In conclusion, deletion of p16Ink4a cells did not negatively impact beta-cell mass and blood glucose under basal and HFD conditions and proliferation was restored in a subset of HFD mice opening further therapeutic targets in the treatment of diabetes.” DOI: https://doi.org/10.18632/aging.204483 Corresponding Author: Cristina Aguayo-Mazzucato - cristina.aguayo-mazzucato@joslin.harvard.edu Keywords: beta cells, mass, proliferation, senolysis, senescence Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204483 About Aging-US: Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://youtube.com/Aging-US LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM